TY  - JOUR
A1  - Möller, Philip
A1  - Overlöper, Aaron
A1  - Förstner, Konrad U.
A1  - Wen, Tuan-Nan
A1  - Sharma, Cynthia M.
A1  - Lai, Erh-Min
A1  - Narberhaus, Franz
T1  - Profound Impact of Hfq on Nutrient Acquisition, Metabolism and Motility in the Plant Pathogen Agrobacterium tumefaciens
JF  - PLOS ONE
N2  - As matchmaker between mRNA and sRNA interactions, the RNA chaperone Hfq plays a key role in riboregulation of many bacteria. Often, the global influence of Hfq on the transcriptome is reflected by substantially altered proteomes and pleiotropic phenotypes in hfq mutants. Using quantitative proteomics and co-immunoprecipitation combined with RNA-sequencing (RIP-seq) of Hfq-bound RNAs, we demonstrate the pervasive role of Hfq in nutrient acquisition, metabolism and motility of the plant pathogen Agrobacterium tumefaciens. 136 of 2544 proteins identified by iTRAQ (isobaric tags for relative and absolute quantitation) were affected in the absence of Hfq. Most of them were associated with ABC transporters, general metabolism and motility. RIP-seq of chromosomally encoded Hfq 3xFlag revealed 1697 mRNAs and 209 non-coding RNAs (ncRNAs) associated with Hfq. 56 ncRNAs were previously undescribed. Interestingly, 55% of the Hfq-bound ncRNAs were encoded antisense (as) to a protein-coding sequence suggesting that A. tumefaciens Hfq plays an important role in asRNA-target interactions. The exclusive enrichment of 296 mRNAs and 31 ncRNAs under virulence conditions further indicates a role for post-transcriptional regulation in A. tumefaciens-mediated plant infection. On the basis of the iTRAQ and RIP-seq data, we assembled a comprehensive model of the Hfq core regulon in A. tumefaciens.
KW  - regulatory small RNAs
KW  - messenger-RNA
KW  - protein HFQ
KW  - bacillus subtilis
KW  - RNA CHAPERONE HFQ
KW  - flagellar basal body
KW  - escherichia coli
KW  - stress resistance
KW  - transport systems
KW  - Erwinia amylovora
Y1  - 2014
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-114874
VL  - 9
IS  - 10
ER  - 
TY  - JOUR
A1  - Wen, Lai
A1  - Feil, Susanne
A1  - Wolters, Markus
A1  - Thunemann, Martin
A1  - Regler, Frank
A1  - Schmidt, Kjestine
A1  - Friebe, Andreas
A1  - Olbrich, Marcus
A1  - Langer, Harald
A1  - Gawaz, Meinrad
A1  - de Wit, Cor
A1  - Feil, Robert
T1  - A shear-dependent NO-cGMP-cGKI cascade in platelets acts as an auto-regulatory brake of thrombosis
JF  - Nature Communications
N2  - Mechanisms that limit thrombosis are poorly defined. One of the few known endogenous platelet inhibitors is nitric oxide (NO). NO activates NO sensitive guanylyl cyclase (NO-GC) in platelets, resulting in an increase of cyclic guanosine monophosphate (cGMP). Here we show, using cGMP sensor mice to study spatiotemporal dynamics of platelet cGMP, that NO-induced cGMP production in pre-activated platelets is strongly shear-dependent. We delineate a new mode of platelet-inhibitory mechanotransduction via shear-activated NO-GC followed by cGMP synthesis, activation of cGMP-dependent protein kinase I (cGKI), and suppression of Ca2+ signaling. Correlative profiling of cGMP dynamics and thrombus formation in vivo indicates that high cGMP concentrations in shear-exposed platelets at the thrombus periphery limit thrombosis, primarily through facilitation of thrombus dissolution. We propose that an increase in shear stress during thrombus growth activates the NO-cGMP-cGKI pathway, which acts as an auto-regulatory brake to prevent vessel occlusion, while preserving wound closure under low shear.
KW  - calcium signalling
KW  - fluorescence imaging
KW  - platelets
KW  - thrombosis
Y1  - 2018
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-233616
VL  - 9
ER  -